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WGU D236 PATHOPHYSIOLOGY EXAM STUDY GUIDE QUESTIONS WITH 100% VERIFIED SOLUTIONSLESSON 1- LESSSON 12

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WGU D236 PATHOPHYSIOLOGY EXAM STUDY GUIDE QUESTIONS WITH 100% VERIFIED SOLUTIONSLESSON 1- LESSSON 12 Lesson 2 : Cellular Response And Adaptation Differentiate between Innate Immunity and Adaptive Immunity. The innate immune system encompasses physical barriers and chemical and cellular defenses. Physical barriers protect the body from invasion. These include things like the skin and eyelashes. Chemical barriers are defense mechanisms that can destroy harmful agent. Examples include tears, mucous, and stomach acid. Cellular defenses of the innate immune response are non specific. These cellular defenses identify pathogens and substances that are potentially dangerous and takes steps to neutralize or destroy them. Adaptive immunity is an organism’s acquired immunity to a specific pathogen. As such, it’s also referred to as acquired immunity. Adaptive immunity is not immediate, nor does it always last throughout an organism’s entire lifespan, although it can. The adaptive immune response is marked by clonal expansion of T and B lymphocytes, releasing many antibody copies to neutralize or destroy their target antigen. 1. What is a way that Adaptive Immunity can recruit innate immunity? The innate immune response to microbes stimulates adaptive immune responses and influences the nature of the adaptive responses. Conversely, adaptive immune responses often work by enhancing the protective mechanisms of innate immunity, making them more capable of effectively combating pathogenic microbes. 3.3. Why are some infections harder on children while other infections are harder on the elderly? Children have not been exposed to many pathogens yet, so they lack memory cells and have not built- up immunity yet. The elderly have a depleted naïve T cell population from years of battling infections, so the likelihood of getting a match is less. 4. Describe how and why our injury response results in the signs of redness, swelling, heat, and pain? Be sure to use chemokines, histamine, and vasodilation in your response. An injury causes an inflammatory response which is responsible for the redness, swelling, heat and pain. Upon injury, cells on the surface begin to release chemokines which act as messengers that something has happened. Mast cells are also alerted to release histamines which travel to the endothelial cells of capillaries and causes vasodilation, which is related to swelling and redness. Vasodilation also causes the capillaries to become leaky which allows for histamines, chemokines and even pathogen particles to enter the blood stream where they are met by neutrophils (non-specific) which start to adhere to the capillary wall and squeeze through the leaky holes (diapedesis or extravasation) to phagocytose pathogens and damaged cells. Dendritic cells just under the surface of skin are also activated to phagocytose foreign particles. Other B cells, T cells (specific) and the complement system also squeeze through the capillary wall to create an area of congestion. 5. Explain dominant vs recessive genetic diseases. What is a "carrier" in recessive genetic diseases? The human genome contains 23 pairs of chromosome (22 autosomes and 1 pair of sex chromosomes). The pairs are homologous and contain the same genes in the same order. This means that every gene has a copy, one inherited from your mother and the other from your father. Not all versions of a gene (alleles) are treated the same by the cell. Some are expressed over others. A dominant gene is a gene that is expressed, even if you only have one copy. The dominant gene will be expressed over the recessive gene, which must have two copies to be expressed. In a dominant genetic disease, all it takes is one copy of the disease to have the disease. Recessive genetic diseases require that the individual gets two copies of the gene to have the disease. Someone who is a carrier for a recessive genetic disease is healthy, but contains a copy of the disease gene, potentially passing it to their offspring. 6. Describe how to determine the probability of clinical outcomes given information about the parents (eg two heterozygous carriers of sickle cell disease) Punnett Squares can be used to determine the potential probabilities of certain traits being passed to offspring. If you know the genotypes of each parent (ie homozygous or heterozygous for the trait), you can determine the possible outcomes. Heterozygous means that the parent has one copy of each gene, homozygous means the parent has the same copy for each gene (either both dominant genes or both recessive genes). 7. What are some of the consequences of alcohol exposure in pregnancy? ND-PAE (neurobehavioral disorder-prenatal alcohol exposure) can cause birth defects and developmental disabilities (fetal alcohol spectrum disorders-FASDs). Affects thinking and memory, causes behavioral issues and linked to trouble with everyday functioning 8. Lesson 3: Musculoskeletal Pathophysiology What are some of the distinctive features associated with trisomy 21, or Down's Syndrome? Why is increased maternal age a risk factor? Distinct features of Down’s syndrome include intellectual disabilities and common physical features that include slanted eyes, flattened bridge of the nose and forehead, short in stature, poor muscle tone, loose joints and single palmar crease. As a woman’s eggs age, they can have mistakes in meiosis potentially leading to a nondisjunction event causing trisomy 21 9. What is Spina Bifida? Why are relative deficiencies in Folic acid or B12 associated with Spina Bifida? Failure to close the neural tube early in gestation due to low folic acid and B-12. These vitamins help activate DNA synthesis in the developing fetus in the first 4 weeks of pregnancy, that are responsible for closing up the spinal column. Three types of spina bifida. 1) spina bifida occulta (most common, less severe) 2) Meningocele (least common) 3) Myelomeningocele (most severe). 10. Essential Question: How does the body's cellular responses and adaptations react to disruptions? The body uses the RAAS system to regulate blood volume and pressure, the immune response reacts to fight infection, the inflammatory response reacts to injury 1. Describe how calcitonin, parathyroid hormone, and calcitriol (Vitamin D) work together to maintain normal blood calcium levels. Pages 926, 968, and 980 of text. Vitamin D: UV light stimulates formation of cholecalciferol, which is hydroxylated in the liver and the kidney into the active form of Vitamin D, calcitriol. Calcitriol stimulates absorption of calcium and phosphorus from the GI tract in the intestine and phosphate in the kidney. Calcitriol increases the calcification of osteoid. Calcitriol also stimulates the formation of bone by raising the levels of calcium and phosphorus in the blood. Low vitamin D levels can cause hypocalcemia, which stimulates the parathyroid gland to release parathyroid hormone (PTH). PTH stimulates osteoclasts to resorb bone calcium to increase blood calcium levels. PTH also stimulates osteoblasts to form bone. PTH stimulates kidneys to reabsorb calcium into the blood and to synthesize vitamin D. When blood calcium gets too high, the thyroid is stimulated to release calcitonin (suppresses osteoclast activity and calcium will be used to form bone). 2. Describe the function of osteocytes within lacunae of bone Osteocytes absorb nutrients from the bloodstream and distribute them within the bone structure. Osteocytes absorb waste products from the bone and excrete them into the bloodstream. 3. Describe bone remodeling. Which cells are involved in this process and what is their function? Osteoclasts breakdown older bone structure and secrete the release calcium into the bloodstream. Osteoblasts absorb calcium from the bloodstream and use it to build new bone structure. Working together, these two cell types allow for regeneration of damaged bone structure. 4. Describe the process of articular degeneration. Which cells are involved in this process and what is their function? Articular Degeneration is the thinning and breakdown of the articular cartilage that covers joints and acts as a lubricant and cushion. This articular cartilage is comprised of chondrocytes in a matrix of collagen and aggrecan. The chondrocytes produce enzymes and other proteins that slowly break down and reform the matrix, allowing for regeneration. Stress caused by being overweight or physical trauma can cause chondrocytes to speed up the matrix breakdown process relative to the reformation process, leading to a thinning of the articular cartilage. 5. What is rickets? How does it develop? Who usually develops rickets? How can rickets be treated? Pages 979-980 of text. Rickets is, primarily, due to a deficiency of vitamin D (due to sunlight exposure), which leads to a deficiency of blood calcium. Rickets can lead to bone weakness, deformity, and susceptibility to fracture. Rickets results from a failure to calcify osteoid due to low amounts of blood calcium and low vitamin D (typically). There are many different types of rickets. Children, especially under age 2, are most likely to be diagnosed with rickets. Infants can develop rickets if their mother's diet was low in vitamin D or in calcium, and breastmilk is low in vitamin D, so mother and baby need to supplement vitamin D (and calcium). The best way to treat rickets is to prevent it by taking supplements of vitamin D and calcium, eating food/drink containing vitamin D/calcium, and getting sufficient sunlight. Physical therapy with weight-bearing exercise can help to treat rickets, as well. It is a multi step process to make the active form of Vit D 6. How does Denosumab treat osteoporosis? Denosumab is a monoclonal antibody that binds to osteoclasts and inhibits their Calcium-withdrawing

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WGU D236 PATHOPHYSIOLOGY
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WGU D236 PATHOPHYSIOLOGY

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WGU D236 PATHOPHYSIOLOGY EXAM STUDY GUIDE
QUESTIONS WITH 100% VERIFIED SOLUTIONSLESSON
1- LESSSON 12

Lesson 2 : Cellular Response And Adaptation

Differentiate between Innate Immunity and Adaptive Immunity.
The innate immune system encompasses physical barriers and chemical and cellular
defenses. Physical barriers protect the body from invasion. These include things like the skin and
eyelashes. Chemical barriers are defense mechanisms that can destroy harmful agent. Examples
include tears, mucous, and stomach acid. Cellular defenses of the innate immune response are non-
specific. These cellular defenses identify pathogens and substances that are potentially dangerous
and takes steps to neutralize or destroy them. Adaptive immunity is an organism’s acquired
immunity to a specific pathogen. As such, it’s also referred to as acquired immunity. Adaptive
immunity is not immediate, nor does it always last throughout an organism’s entire lifespan,
although it can. The adaptive immune response is marked by clonal expansion of T and B
lymphocytes, releasing many antibody copies to neutralize or destroy their target antigen.

1. What is a way that Adaptive Immunity can recruit innate immunity?
The innate immune response to microbes stimulates adaptive immune responses and
influences the nature of the adaptive responses. Conversely, adaptive immune responses often work
by enhancing the protective mechanisms of innate immunity, making them more capable of
effectively combating pathogenic microbes.

3.3. Why are some infections harder on children while other infections are
harder on the elderly?

Children have not been exposed to many pathogens yet, so they lack memory cells and have not built-
up immunity yet. The elderly have a depleted naïve T cell population from years of battling infections, so the
likelihood of getting a match is less.

4. Describe how and why our injury response results in the signs of
redness, swelling, heat, and pain? Be sure to use chemokines, histamine, and
vasodilation in your response.
An injury causes an inflammatory response which is responsible for the redness, swelling,
heat and pain. Upon injury, cells on the surface begin to release chemokines which act as
messengers that something has happened. Mast cells are also alerted to release histamines which
travel to the endothelial cells of capillaries and causes vasodilation, which is related to swelling
and redness. Vasodilation also causes the capillaries to become leaky which allows for histamines,
chemokines and even pathogen particles to enter the blood stream where they are met by
neutrophils (non-specific) which start to adhere to the capillary wall and squeeze through the leaky
holes (diapedesis or extravasation) to phagocytose pathogens and damaged cells. Dendritic cells
just under the surface of skin are also activated to phagocytose foreign particles. Other B cells, T
cells (specific) and the complement system also squeeze through the capillary wall to create an
area of congestion.

,5. Explain dominant vs recessive genetic diseases. What is a "carrier" in
recessive genetic diseases?
The human genome contains 23 pairs of chromosome (22 autosomes and 1 pair of sex
chromosomes). The pairs are homologous and contain the same genes in the same order. This means
that every gene has a copy, one inherited from your mother and the other from your father. Not
all versions of a gene (alleles) are treated the same by the cell. Some are expressed over others. A
dominant gene is a gene that is expressed, even if you only have one copy. The dominant gene will
be expressed over the recessive gene, which must have two copies to be expressed. In a dominant
genetic disease, all it takes is one copy of the disease to have the disease. Recessive genetic
diseases require that the individual gets two copies of the gene to have the disease. Someone who
is a carrier for a recessive genetic disease is healthy, but contains a copy of the disease gene,
potentially passing it to their offspring.

6. Describe how to determine the probability of clinical outcomes given
information about the parents (eg two heterozygous carriers of sickle cell
disease)
Punnett Squares can be used to determine the potential probabilities of certain traits
being passed to offspring. If you know the genotypes of each parent (ie homozygous or
heterozygous for the trait), you can determine the possible outcomes. Heterozygous means that
the parent has one copy of each gene, homozygous means the parent has the same copy for each
gene (either both dominant genes or both recessive genes).

7. What are some of the consequences of alcohol exposure in
pregnancy?
ND-PAE (neurobehavioral disorder-prenatal alcohol exposure) can cause birth defects and
developmental disabilities (fetal alcohol spectrum disorders-FASDs). Affects thinking and memory,
causes behavioral issues and linked to trouble with everyday functioning

8. What are some of the distinctive features associated with trisomy 21,
or Down's Syndrome? Why is increased maternal age a risk factor?
Distinct features of Down’s syndrome include intellectual disabilities and common physical features
that include slanted eyes, flattened bridge of the nose and forehead, short in stature, poor muscle tone, loose
joints and single palmar crease. As a woman’s eggs age, they can have mistakes in meiosis potentially leading
to a nondisjunction event causing trisomy 21

9. What is Spina Bifida? Why are relative deficiencies in Folic acid or
B12 associated with Spina Bifida?
Failure to close the neural tube early in gestation due to low folic acid and B-12. These vitamins help
activate DNA synthesis in the developing fetus in the first 4 weeks of pregnancy, that are responsible for
closing up the spinal column. Three types of spina bifida. 1) spina bifida occulta (most common, less severe)
2) Meningocele (least common) 3) Myelomeningocele (most severe).

10. Essential Question: How does the body's cellular responses and
adaptations react to disruptions?
The body uses the RAAS system to regulate blood volume and pressure, the immune response
reacts to fight infection, the inflammatory response reacts to injury


Lesson 3: Musculoskeletal
1. Describe
Pathophysiology how calcitonin,
parathyroid

, hormone, and calcitriol (Vitamin D) work together to maintain normal
blood calcium levels.

Pages 926, 968, and 980 of text. Vitamin D: UV light stimulates formation of cholecalciferol, which
is hydroxylated in the liver and the kidney into the active form of Vitamin D, calcitriol. Calcitriol
stimulates absorption of calcium and phosphorus from the GI tract in the intestine and phosphate in
the kidney. Calcitriol increases the calcification of osteoid. Calcitriol also stimulates the formation of
bone by raising the levels of calcium and phosphorus in the blood. Low vitamin D levels can cause
hypocalcemia, which stimulates the parathyroid gland to release parathyroid hormone (PTH). PTH
stimulates osteoclasts to resorb bone calcium to increase blood calcium levels. PTH also stimulates
osteoblasts to form bone. PTH stimulates kidneys to reabsorb calcium into the blood and to synthesize
vitamin D. When blood calcium gets too high, the thyroid is stimulated to release calcitonin
(suppresses osteoclast activity and calcium will be used to form bone).
2. Describe the function of osteocytes within lacunae of bone
Osteocytes absorb nutrients from the bloodstream and distribute them within the bone structure.
Osteocytes absorb waste products from the bone and excrete them into the bloodstream.

3. Describe bone remodeling. Which cells are involved in this process and
what is their function?
Osteoclasts breakdown older bone structure and secrete the release calcium into the bloodstream.
Osteoblasts absorb calcium from the bloodstream and use it to build new bone structure. Working together,
these two cell types allow for regeneration of damaged bone structure.

4. Describe the process of articular degeneration. Which cells are involved
in this process and what is their function?
Articular Degeneration is the thinning and breakdown of the articular cartilage that
covers joints and acts as a lubricant and cushion. This articular cartilage is comprised of
chondrocytes in a matrix of collagen and aggrecan. The chondrocytes produce enzymes and
other proteins that slowly break down and reform the matrix, allowing for regeneration. Stress
caused by being overweight or physical trauma can cause chondrocytes to speed up the matrix
breakdown process relative to the reformation process, leading to a thinning of the articular
cartilage.

5. What is rickets? How does it develop? Who usually develops rickets? How
can rickets be treated?
Pages 979-980 of text. Rickets is, primarily, due to a deficiency of vitamin D (due to sunlight
exposure), which leads to a deficiency of blood calcium. Rickets can lead to bone weakness, deformity, and
susceptibility to fracture. Rickets results from a failure to calcify osteoid due to low amounts of blood calcium
and low vitamin D (typically). There are many different types of rickets. Children, especially under age 2, are
most likely to be diagnosed with rickets. Infants can develop rickets if their mother's diet was low in vitamin D
or in calcium, and breastmilk is low in vitamin D, so mother and baby need to supplement vitamin D (and
calcium). The best way to treat rickets is to prevent it by taking supplements of vitamin D and calcium, eating
food/drink containing vitamin D/calcium, and getting sufficient sunlight. Physical therapy with weight-bearing
exercise can help to treat rickets, as well. It is a multi step process to make the active form of Vit D

6. How does Denosumab treat osteoporosis?
Denosumab is a monoclonal antibody that binds to osteoclasts and inhibits their Calcium-withdrawing
capability.

7. Distinguish between open reduction and internal fixation (ORIF) and hip
replacement surgery.
Open reduction and internal fixation involves “surgical opening’ and insertion of hardware into the
patient that assists with maintaining proper bone alignment during the healing process. Hip replacement
involves replacement of a fractured hip joint with a prosthesis.

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